Download Fatal asthma in a young ... hyperresponsiveness but stable peak flow ...

Eur Respir J
CASE REPORT
1989, 2. 1006-1012
Fatal asthma in a young patient with severe bronchial
hyperresponsiveness but stable peak flow records
M. Saetta, G. Thiene", S. Crescioli, L.M. Fabbri
Fatal asthma in a young patienJ with severe bronchial hyperresponsiveness but
stable peak flow records. M. Saetra, G. Thiene, S. Crescioli, LM. Fabbri.
ABSTRACT: We report the sudden death of a 16 yr old boy with asthma.
At presentation, the patient had symptoms of active asthma, mild
bronchoconstrlctlon, severe airway hyperresponsiveness to methacholine,
and Increased variability of peak expiratory flow records. After the patient
was placed on Inhaled bec:lomethasone (1 mg b.i.d preceded by inhaled
fenoterol 0.4 mg b.i.d) he rapidly felt better, lung function Improved, but
airway responsiveness remained severe. Four months later, on the day he
died, he was well until a fatal attack or asthma occurred around midnight
without Identifiable precipitating factors. Taken to hospital, he was dead
on arrival. Necroscopy and mlcroscopy showed the characteristic features
or asthma death. This case report suggesl'i that; a) asthma death may
occur suddenly and unexpectedly; b) asthma death may not be prevented
by long-tenn treatment with high-dose Inhaled beclomethasone; c) severe
bronchial hyperresponslveness, even in the presence of stable peak flow
records, may Identify asthmatic patients at risk of sudden death.
Eur Respir J., 1989, 2, 1008-1012.
Bronchial asthma affects 3-5% of the population [1],
and deaths from asthma, although uncommon, have
received increasing attention for several reasons. A
significant increase of asthma deaths, particularly in young
people, has been reported in some countries such as the
United Kingdom [2) and New Zealand [3), at a time
when the advances made in the understanding of the
pathogenetic mechanisms of asthma and the introduction
of many effective therapeutic agents were expected to
improve the prognosis of the disease.
There is some agreement that most deaths from asthma
can be attributed to inadequate assessment and/or inadequate treatment [4), and there is a belief that asthma
deaths might indeed be prevented by avoiding the triggering factors, when known, and by instructing patients
and physicians to face the severity that the disease may
achieve by using appropriate treatment [4, 5]. Prophylaxis of severe attacks is also important; treatment that
reduces diurnal variations of airflow obstruction may
decrease the risk of sudden death, since patients with a
large diurnal variation are at greatest risk [5-8].
We hereby report the case of a young patient with
asthma who died suddenly, despite the fact that
pharmacologic treatment with inhaled steroids and
bronchodilators was able to control symptoms and
circadian variations in airflow limitation for weeks.
Institute of Occupational Medicine, University of
Padova and •Dept of Pathology, University of
Padova, Italy.
Correspondence: M. Saeua, Istituto di Medicina del
Lavoro, Universita' degli Studi di Padova, Via Jacopo
Facciolati 71, 35127 Padova, Italy.
Keywords: Asthma; airway responsiveness; inflammation, fatal asthma.
Received: 22 January, 1989; accepted after revision 9
August, 1989.
Presented at the Annual Meeting of the Societas
Europaea Physio1ogiae Oinicac Rcspiratoriae, Athens,
20-24 June, 1988.
Supponed by Italian National Research CoWtcil (Grants
No. 87.00215.04 and 87.00266.56), by the Italian
Ministry of Education, and by the European
Community for Coal and Steel.
Case Report
A 16 yr old boy with a 13 yr history of asthma had
been treated in the previous month with inhaled
fenoterol (400 JJ.g b.i.d) and inhaled bcclomethasone (1
mg b.i.d), and was well until a few minutes before a fatal
asthma attack occurred on November 17, 1987, around
midnight.
Past history included infant eczema, bronchial asthma
from the age of 3 and a positive skin test for grass pollen,
Dermatophagoides pteronissinus and Dermatophagoides farinae. Radioallergosorbent test was positive
for grass pollen and negative for mites. Family history
was positive for atopy and allergic rhinitis, but not for
asthma. Immunotherapy with grass pollen was performed
from 1979 to 1983, and did not provide significant benefits
or local or systemic reactions. The patient was not .known
to have any drug sensitivities, history of aspirin-induced
asthma, rhinitis, or food allergy. Parents excluded addiction to any drug. In the last five years he had 1 to 2
severe asthma attacks per year and frequent episodes of
mild dyspnoea with wheezing during the night in the
summer-fall season. He also had exercise-induced asthma.
Until August, 1987, when he was admitted to our
Asthma clinic, he was treated regularly with theophylline (Theo-Dur 200 1 tablet in the evening) and
1009
FATAL ASTHMA
The patiem was instructed to use Llle peak fl ow meter
and to record peak expiratory flow rate (PEFR), symptoms, and therapy in lhe daily diary card. He was asked
to record PEFRs at 7.00, 10.00, 14.00, 18.00, and 22.00
h, and to report measurements obtained shortly after bronchodilator (when needed) to assess the reversibility of
bronchoconstriction. The variability of PEFR was
calculated as described by RYAN et al. [10]. i.e. the
difference between the maximum and minimum PEFR
of each day expressed as a percentage of the max imum.
The reversibility to fenoterol was calc ulated as the
percentage ratio between the PEFR value after the inhaImion and the closcsLPEFR value before the inhalation
of fenoterol.
The patient was recommended to use regularly inhaled
ste roids (bcclome thasone dipropionate, Clc nil Forte,
Chiesi, Parma, 0.5 mg b.i.d), and inhaled fenoterol only
when required. During the first 4 days of treatment PEFRs
remained highly variable (the mean variability of the four
days was 32%), and Llle reversibility to fenoterol reached
62% (fig. la). Already during the follow ing week (fo ur
days are represented in fig. lb) the patient reported a
significant improvement of symptoms, PEFR increased,
and t11e diurnal variation of PEFRs decreased (the mean
variability of the four days was 13%, a value very similar to the mean variability found in non-asthmatic
subjects [10}), but occasional morning dip was still present
(fig. lb).
with inhaled fenoterol, and with oral steroids during
exacerbations. On August 10, 1987, when he came to
our Clinic complaining of asthma symptoms, spirometry
and inhalation challenges with methacholine were
performed. Spirometry demonstrated mild bronc hoconstriction (vital capac ity) (VC = 5.0 I, 93% predicted;
forced expiratory volume in one second (FEY,)= 3.7 /,
79% predicted) and inhalation c hallenge with methacholine revealed extremely severe airway hypcrresponsiveness (provocative dose of methacholine caus ing a 20%
decrease in FEV 1 (PD 20 FEY,) methacholine <0.02 mg).
Airway responsiveness to methacholine aerosol was
assessed willl the dosimeter method as previously described [9]. With this method airway responsiveness is
considered extremely severe if PDw FEY, is less than
0.02 mg, severe if PD20 FEV 1 is between 0.02 and 0.1
mg, moderate if PD 20 FEV1 is between 0.1 mg and 0.7
mg, and normal above 1.4 mg.
The patiem was advised to buy a peak flow me ter
(Assess, Health Scan Products Inc., Cedar Grove, NJ)
and the appropriate diary (Agendasma, Markos,
Monza, Italy), and to return to our CLinic in one week.
On the 2nd of September, 1987, his lung volumes were
unchanged (VC= 5.4 /, 100% predicted; FEY,= 3.8 /,
80% predicted), but at Llle inhalation challenge he
reacted to the inhalation of the diluent phosphate buffer
saline (FEY 1 fall = 22%) so that Llle test could not be
completed.
Beginning of
treatment
PEFR
/-min·'
a
Beclomethasone 0.5 mg b.l.d Beclomethasone 1 mg b.l.d
Fenoterol when required b
Fenoterol 0.4 mg b.i.d c
70 0
600
- ,
f--r
1
~-
500
-- -- --
-V
tt + 11"
~
I
I
·-
400
- ~ 1\: -- j -'
- - - ·;\11 - --- -- -- --.
-
- I-
... l!
t.
'~
'
-
-
-
,
'
'
- 'I - ~L \I/ -- -- - --. - - - - --"
-- --- -- - - - -- -.--- ~1- -
1- -
lOO
-
- I-
'
tO t • tt JJ
r
lO \4 U U
f
tO • • U
U
f
tO M lt Jl f
'0 '4 i t U
t 10 it
tl 11
I
tO 14 U JJ f
tO 14 If 1 1 J IQ 14 t l 1) f
tO 114
t1 U
t
tO 14 il U
I
¥.Ji ' ' If 1 I t
Hours
Fig. I.- Peak expiralory Oow rares (PEFR) at 7.00, 10.00, 14.00 and 22.00 hours during the first four days of treatml.lnt (panel a), during four
days of the following wcc.k (panel b), and during the last four days before the fatal attack (panel c). Doned lines and asterisks represent the
reversibility to fenoterol. ·fhc dnily variability of PET=R calculated as described in the text was: 4 1%, 26%. 20% and 39%. mean value= 32%, in
panel a: 14%. 21%, 7% and 10%. mean value= 13%. in panel b: 17%, 13%, 10%, and 14%, mean value= 14%, in panel c. The reversibility
to fen01erol. calculated a.s described in the text, was: 62% and 35%, mean value= 49% in panel a; 23%, 7%, 13%, 9%, 9%, 10%, 14% and 11%,
mean value = 12% in panel c.
1010
M. SAETTA ET AL.
On October 7, 1987, spirometric values had almost
completely returned to within normal values (VC=5.5 /,
103% predicted; FEV1=4.2 /, 88% predicted); however,
at variance with previous measurements, FEV1 progressively decreased with forced manoeuvres alone (FEV1
decreased from 4.2, to 3.6, and 3.2 in the three blows).
Thus, again, the inhalation challenge with methacholine
could not be performed, and, because this was interpreted
as a sign of marked airway hyperresponsiveness, treatment was changed (fenoterol 0.4 mg b.i.d, to be taken
before beclomethasone; beclomethasone increased to 1
mg b.i.d).
In the month before the fatal attack, he did not complain of asthma symptoms or exercise-induced asthma.
He reported a cold around the end of October, but this
event was not associated with asthma symptoms or with
changes in PEFRs. In the four days before the fatal attack
(fig. le) the values of PEFR ranged between 480 and
600 /·min·1 , and the mean variability of the four days was
14%. During the same days the patient regularly took the
usual medications, and the mean daily reversibility to
fenoterol was around 12% (fig. le).
On November 17, 1987, the day he died, in the morning he ran for about two miles because he missed the bus
and was late for school. He did not report symptoms or
additional medications in the diary, his PEFRs ranged
between 500 and 580 /·min-• during the day, and the
reversibility to fenoterol was 14% at 7.00 and 11% at
14.00 (fig. le). He took the usual medications (last dose
of fenoterol and inhaled steroid at 18.00), and after a
light dinner he went to bed around 22.00. His mother
saw the patient sleeping well around midnight, and his
breathing seemed normal to her. About 30 min later she
heard the patient stepping into the bathroom where he
kept his medicines: then she heard 4 actuations of a
pressurized cannister, then identified to contain fenoterol. By the time she came to see him, he was $ready
heavily dyspnoeic and unable to speak. The mother felt
that he was already dead at home within 15 min. Taken
by the father to the nearest hospital, he was dead on
arrival.
Necroscopy excluded cerebral or cardiovascular causes
of death. The lungs were overintlated. Specimens from
different lobes were obtained after fixation in 10%
formaldehyde in saline. Specimens were embedded in
paraffin wax, sections 7 )J.ffi thick were cut and stained
with haematoxylin-eosin. Microscopy showed scattered
alveolar oedema, oedematous thickening of the bronchial
walls associated with dilatation of the bronchial vessels,
mucous plugs with desquamed epithelial cells suboccluding most of the airways (fig. 2a), denudation of airway
epithelium, marked thickening of the basement membrane
(fig. 2b), smooth muscle hypertrophy and inflammatory
infiltrate, including eosinophils, mainly in the outer layer
of the airway walls.
Discussion
Fig. 2. - Panel a: cross-section of a cartilagineous bronchus occluded
by muoous plug. Nodular inflammatory infiltrates are seen in the outer
layer of the bronchial wall. Stain: haematoxylin-eosin; Panel b: detail
of panel a, showing marked thickening of the basement membrane,
oedema dissociating the smooth muscle cells, and scattered inflammatory infiltrates. Stain: haematoxylin-eosin.
This paper reports a fatal attack of asthma in a young
patient who was well-controlled by regular treatment with
inhaled steroids and beta-agonists. He complained of no
symptoms and his peak flow records had been quite stable
in the last month before death, but he had an extremely
severe degree of airway hyperresponsiveness which was
not affected by therapy. Death occurred suddenly without premonitory symptoms or signs. The fatal attack was
so sudden and progressed so rapidly that appropriate
medical help could not be given in time. Previous reports
have emphasized that up to one quarter of deaths from
asthma occur within 30 min of onset of the attack [11],
and that there are children with apparently trivial asthma
who are at risk of sudden death [12].
In the present report two recent events could be related
to the fatal outcome. Firstly, the patient had an infection
of the upper airways, probably viral, about three weeks
before. That episode was not associated with obvious
exacerbation of asthma, as suggested by the records
showing that peak flows were unchanged, and he did not
require additional therapy. Recent editorials do not
mention viral infection as a risk factor for fatal asthma
[4, 5, 13]. Secondly, the patient underwent strenuous
exercise in the morning of the day he died; he had run
1011
FAT AL ASTHMA
for about two miles because he had missed the bus and
was late for school. Howe ver, he d id not report symptoms or additiona l medications in the diary, and the peak
expiratory flow rate was 500 /·min·• at 07.00 and 580
/·min·• at 10.00, i.e before and after the run. Several papecs
reponed late asthmatic reactions after exercise, and indeed
some of these reactions may occur with several hours
delay [14), but it is still doubtful whe ther such reactions
are indeed due to exerc ise or to withdrawal of therapy
[15, 16]. Whether or not the morning's strenuous exercise may have been the cause of the fatal attack remains
uncertain.
Airway hyperresponsiveness is believed to reflect the
severity of asthma, both because it corre lates with the
amount of medication required to comrol symptoms [17],
and because it corre lates with the moming dips and the
diurnal variations of PEFRs [101. This correlation is
pro bably true for most asthmatic subjectS but, unfortunately, this was not tl1e case for the patient reported here.
In fact, after he started regular therapy, his PEFRs
increased and diumal variation decreased to the levels
found in non-asthmatic subjects [ 10), even if tlle degree
of bro nchiaJ hyperresponsiveness re mained extreme ly
severe.
Indeed, tlle most striking functional finding in this
patient was the severe bronchial hyperrespo nsiveness,
bronchoconstriction being triggered even by inhalation
of an extremely low dose of metllacholine, phosphate
buffer saline solutio n, o r deep inspiration. WooLCOCK et
al. [ 18] have studied bronchial responsiveness in patients
who had a "near-miss deatl1" from asthma. At tlle time
of tlle study, 3 to 10 weeks after the nearly fatal attack,
all patie nts had FEV 1 above 70% of the predicted value,
but all had severe bronchial hyperresponsiveness, wi tll
PD 20 FE V , values less than 0.1 ).lmo l of hista mine
(i.e. less than 0.25 mg·ml' 1 with the Canadian pro tocol
[19), less than 2.5 unit witll the Nortll American protocol
[20], and less tllan 0.01 mg with o ur protocol [9]), and
extreme steepness of tlle dose-response curves. The
authors attempted to decrease the severity of bronchial
bypcrreac ti vity in these patients by using aggressive therapy based on high dose steroids. The three patients in
whom airway responsiveness significantly decreased afte r
therapy s urvived, whereas tlle two patients in whom
airway responsive ness did not change subsequently had
a fatal auack. From this experience, Wootcocx suggests
tha t tlle severity of bro nchial hyperresponsiveness must
be considered the most important risk factor of fata l
astllma, and that adequate treatment, particularly with
oraJ and topical s te roids [21, 22), must be attempted to
decrease tlle seve rity of airway responsiveness.
Altllough we did not give oral steroids, we observed
that high dose inhaled beclomethasone ( 1 mg b.i.d) taken
reg ularly by tlle patient was able to contro l sympto ms
and improve PEFRs, and thus we considered asthma under
contro l. Howe ve r, re trospecti vely, because o f the
outcome of this case, we suggest that a course of ora l
steroids should be considered in patients with severe
bronchial hyperresponsiveness.
The patient described used regularly inhaJed fenoterol
(400 J,lg b.i.d) and recorded PEFRs before and after in-
haJation. Asthma deaths have been related in the past to
abuse of bronchodilator aerosols [23 , 24), and such abuse
could be due to development of tachyphylaxis [25). In
the present case, abuse of fenoterol could be excluded
from the dosage carefully reported in the diary, and tachyphylaxis can be excluded by the observation tllat on the
day he died be reported an increase of PEFR after fenoterol similar Lo that in the previous days both in the
morning and at 14.00 (fig. le). However, a recent paper
relates asthma death in New Zealand to tlle use of fenoterol by metered dose inhaler [26).
Oedema of the airway walls and mucous plugs were
the prominent features of lung patho logy. Although betaagonists are first choice potent bronchodilato rs and must
be used to treat acute asthma, they do not a ffect vascular
penneability [27] , and therefore they may not decrease
bronchial oedema. The pathology and the outcome of
this case may reinforce the suggestion that adrenaline, an
agent witll vasoconstrictor effects due to stimulation of
alpha receptors in addition to beta receptors, should be
used in particularly severe attacks of asthma not reversed
by the usual therapy [7, 28]. In tllis case the fatal attack
developed and progressed so rapidly tllat appropriate
medical help could not be given in Lime, and previous
reports have emphasized that up to one quarter of deatlls
from asthma occur within 30 min of onset of the attack
[11]. We wonder whether appropriate education of patients at risk of sudden astllma death to carry emergency
sets including aerosol bronchodilators, adrenaline and
steroids, and appropriate training to use them, and particularly to take adrenaline, might help to reduce the
number of sudden astllma deaths [7).
Microscopic examination of the lungs showed some
characteristic features of asthma death [29- 31 ]: mucous
plugs suboccluding most of the airways, oedematous
thickening of the bronchial walls associated with dilatation of the bronchial vessels, denudation of airway epithelium, marked tllickening of the basement membrane,
smooth muscle hypertrophy and inflammatory infiltrate,
including eosinophils, mainly in the outer layer of the
airway walls. Among all tllese features, the most striking
microscopic finding was the excess of secretions and
tissue swelling due to oedema of tlle bronchial walls. As
pointed out by MoRENO et al. [32), in tllese conditions of
organic bronchial obstruction, even a small smootll muscle
contraction could produce an amplified inc rease in
resistance tllat in turn may contribute to tlle fatal event.
Acknowledgements: We thank Dr. L Tolin for revising and typing the manuscript.
References
I. Mc Fadden ER. Ausren KF.- Asthma. In: Hw:r:ison's principles of internal medicine, 11th ed. E. Braunwald, K.J.
Isselbacker, K.G. Pet.ersdorf, J.D. Wilson, J.B. Martin, A.S.
Fauci eds, McGraw-Hill. New York, 1987, pp. 1060-1065.
2. M orrison Smith J, Harding LK, Cumming G. - The
changing prevalence of asthma in school children. Clin
Allergy, 1971, 1, 57- 61.
1012
M. SAETIA ET AL.
3. Mit.chell E. -Increasing prevalence of asthma in children.
NZ Med J, 1983, 96, 463-464.
4. Benatar SR. - Fatal asthma. N Engl J Med, 1986, 314,
423-429.
5. Shcffer AL, Buist AS (Eds). -Proceedings of the asthma
mortality task force. J Allergy Clinlmmunol, 1987, 80,361-514.
6. Hetzel MR, Clark TJH, Branthwaite MA. - Asthma:
analysis of sudden deaths and ventilatory arrests in hospital. Br
Med J, 1977, 1, 808-811.
7. Bateman JRM, C!arke SW. - Sudden death in asthma.
Thorax, 1979, 34, 40-44.
8. Westerman DE, Benatar SR, Potgieter PD, Ferguson AD.
- Identification of the high-risk asthmatic patient: experience
with 39 patients undergoing ventilation for status asthmaticus.
Am J Med, 1979, 66, 565-572.
9. Mapp C, Boschetto P, Dal Vecchio Let al. -Protective
effect of antiasthma drugs on late asthmatic reactions and
increased airway responsiveness induced by toluene diisocyanate in sensitized subjects. Am Rev Respir Dis, 1987, 136,
1403-1407.
10. Ryan G, Latimer KM, Dolovich J, Hargreave FE. Bronchial responsiveness to histamine: relationship to diurnal
variation of peak flow rate, improvement after bronchodilator,
and airway calibre. Thorax, 1982, 37, 423-429.
11. Macdonald JB, Seaton A, Williams DA. -Asthma deaths
in Cardiff, 1963-1974: 90 deaths outside hospital. Br Med J,
1976, 1, 1493-1495.
12. Colin F, Robertson F, Bowes G, Rubinfeld A.- Sudden
death in pediatric asthma. Am Rev Respir Dis, 1989, 139, A130.
13. Li JTC, O'Connel EJ.- Viral infections and asthma. Ann
Allergy, 1987, 59, 321-333.
14. Lee TH, O'Hickey SP.- Exercise induced asthma and late
phase reactions. Eur Respir J, 1989, 2, 195-197.
15. McFadden ER. - Exercise and asthma. N Engl J Med,
1987, 317, 502-504.
16. Rubinstein I, Levison H, Slutsky AS, Hak H, Wells J,
Zamel N, Rebuck AS. - Immediate and delayed bronchoconstriction after exercise in patients with asthma. N Engl J Med,
1987, 317, 482-485.
17. Hargreave FE, Ryan G, Thomson NC, O'Byme PM,
Latimer K, Juniper EF, Dolovich J. - Bronchial responsiveness
to histamine or methacholine in asthma: measurement and
clinical significance. J Allergy Clin /mmunol, 1981, 68, 347-355.
18. Drazen GM, Boushey HA, Holgate ST, Kaliner M,
O'Byme P, Valentine M, Widdicombe JH, Woolcock A. - The
pathogenesis of severe asthma: a consensus report from the
workshop on pathogenesis. J Allergy Clin lmmunol, 1987, 80,
428-437.
19. Ryan G, Dolovich MB, Roberts RS et al.- Standardization of inhalation provocation tests: two techniques of aerosol
generation and inhalation compared. Am Rev Respir Dis, 1981,
123, 195-199.
20. Chai H, Farr RS, Froehlich LA et al. -Standardization of
bronchial inhalation challenge procedures. J Allergy Clin
lmmunol, 1975, 56, 323-327.
21. Kerrebijn KF, van Essen-Zandvliet EEM, Neijens HJ. Effect of long-term treatment with glucocorticosteroids and
beta-agonists on bronchial responsiveness in asthmatic
children. In: Glucoconicosteroids inflammation and bronchial
hyperreactivity. Hogg JC, Ellul-Michalleff R, Brattsand R, eds.
Amsterdam, Excerpta Medica. 1985, pp. 104-109.
22. Dutoit n, Salome CM, Woolcock AI. - Inhaled corticosteroids reduce the severity of bronchial hyperresponsiveness in
asthma but oral theophillyne does not. Am Rev Respir Dis,
1987, 136, 1774-1778.
23. Greenberg MJ, Pines A. - Pressurised aerosol in asthma.
Br Med J, 1967, 1, 563.
24. Douglas EM, Hillier T, Johnson IC.- Pressurised aerosols
in asthma. Br Med J, 1967, 2, 53.
25. Reed CE, Kemp JP, Pierson WE. - A report from the
workshop on pharmacology: beta-adrenergic agonists. J Allergy
Clin Jmmunol, 1987, 80, 442-443.
26. Crane J, Flatt A, Jackson R, et al. - Prescribed fenoterol
and death from asthma in New Zealand, 1981-83: case-control
study. LallCet, 1989, i, 917-922.
27. Boschetto P, Roberts NM, Rogers DF, Bames PJ.- Effect
of anti-asthma drugs on microvascular leakage in guinea-pig
airways. Am Rev Respir Dis, 1989, 139, 416-421.
28. Coupe MO, Guly 0, Brown E, Bames PJ. - Nebulised
adrenaline in acute severe asthma: comparison with salbutarnol.
Eur J Respir Dis, 1987, 71, 227-232.
29. Dunnil MS. - Problems in the pathology of asthma. Bull
Eur Physiopathol Respir, 1986, 22 (Suppl. 7), 9-11.
30. Hogg JC.- The Pathology of asthma. In: Bronchial asthma.
Weiss SB, Barsan GC, Segal MS, Stein M, eds. Boston, Little,
Brown, 1985, pp. 209-217.
31. Saetta M, Danieli D, Fabbri LM, Allegra L. - Pathology
of bronchial asthma and animal models of asthma. Eur Respir
J, 1989, 2, Suppl 6, 477s-482s.
32. Moreno RH, Hogg JC, Pare PD. - Mechanics of airway
narrowing. Am Rev Respir Dis, 1986, 133, 1171-1180.
Asthme mortel chez un jeune patient avec hyperreactivite
brollChique severe, mais valeurs stables du debit de pointe.
Observation clinique. M. Saetta, G. Thiene, S. Crescioli, L.M.
Fabbri.
RESUME: Nous faisons etat de la mort subite d'un gar~n de
16 ans attcint d'asthme. A !'admission, le patient avait des
symptomes d'asthme evolutif, une bronchoconstriction legere,
un hyperreactivite sev~re des voies aeriennes a la Methacholine, et une augmentation de la variabilite des valeurs du debit
de pointe. Apr~s traitement a la beclomethasone en inhalation
(1 mg 2 fois par jour precede par 0.4 mg de fenoterol 2 fois par
jour), il s'est senti rapidement ameliore, la fonction pulmonaire
s'est amelior&, mais la reactivite bronchique restait severe.
Quatre mois plus tard, le jour de sa mort, il s'est senti bien
jusqu'a ce que la crise d'asthme letale survenionne vers minuit,
sans aucun facteur precipitant identifiable. 11 etait mort a
l'arrivee a l'hopital. L'autopsie et l'examen microscopique ont
montre lcs signes caracteristiques de la mort dans l'asthme.
Cette observation sugg~re que la mort dans l'asthme peut survenir de fa~on soudaine et inattendue, que la mort dans
l'asthme peut ne pas etre prevenue par un traitement prolonge
meme avec de fortes doses de beclomethasone en inhalations,
et qu'unc hyperreactivite bronchique severe meme avec des
debits de pointe stables peut identifier les patients asthmatiques
a haut risque d'un deces par asthme.
Eur Respir J. , 1989, 2, 1008-1012.